Aliskiren reduced renal fibrosis in mice with chronic ischemic kidney injurybeyond the direct renin inhibition

Chiao Yin Sun, Wen Jin Cherng, Hui Zhen Jian, Hsiang Hao Hsu, I. Wen Wu, Heng Jung Hsu, Mai Szu Wu

Research output: Contribution to journalArticlepeer-review

19 Citations (Scopus)


Chronic renal ischemia leads to renal fibrosis and atrophy. Activation of the renin-angiotensin-aldosterone system is one of the main mechanisms driving chronic renal ischemic injury. The aim of the present study was to define the effect of aliskiren in chronic ischemia of the kidney. Two-kidney, one-clip mice were used to study chronic renal ischemia. Aliskiren significantly lowered the blood pressure in mice with renal artery constriction (92.1±1.1 vs. 81.0±1.8 mm Hg, P<0.05). Renin expression was significantly increased in ischemic kidneys when treated with aliskiren. In addition, (Pro)renin receptor expression was decreased by aliskiren in ischemic kidneys. Aliskiren treatment significantly increased klotho expression and reduced the expression of fibrogenic cystokines, caspase-3 and Bax in ischemic kidneys. Histological examination revealed that aliskiren significantly reduced the nephrosclerosis score (4.5±1.9 vs. 7.3±0.4, P<0.05). Immunofluorescence staining also showed that aliskiren decreased the deposition of interstitial collagen I in ischemic kidneys. In conclusion, direct renin inhibition significantly reduced renal fibrosis and apoptosis following chronic renal ischemia.

Original languageEnglish
Pages (from-to)304-311
Number of pages8
JournalHypertension Research
Issue number3
Publication statusPublished - Mar 2012
Externally publishedYes


  • chronic renal ischemia
  • direct renin inhibitor
  • renal fibrosis
  • renin-angiotensin-aldosterone system

ASJC Scopus subject areas

  • Internal Medicine
  • Physiology
  • Cardiology and Cardiovascular Medicine


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